HYPERGLYCEMIC CRISIS

Diagnostic Criteria for DKA and HHS

DKA is distinguished by a blood glucose of >250 mg/dL, moderate ketonuria or

ketonemia, arterial pH of <7.3, and a bicarbonate of <15 mEq/L (1). A diagnosis of HHS
may be presumed in a diabetic patient with an altered sensorium, severely elevated
glucose (usually >600 mg/dL), minimal or no ketonuria or ketonemia, serum osmolality
>320 mOsm/kg, arterial pH (typically) >7.3, and a bicarbonate of >15 mEq/L

Pathophysiology

Insulin stimulates hepatocellular glucose uptake, glycogen storage, and lipogenesis.

DKA and HHS are severe complications of DM

A combination of hormonal imbalances causes DKA  In the setting of insulin deficiency,

increased glucagon, catecholamines, cortisol, and growth hormones lead to
increased extracellular glucose, decreased glucose use, and hyperglycemia

These counter-regulatory and

stress hormones stimulate lipolytic pathways, and the resultant free fatty acids are
oxidized to ketone bodies, such as acetone, acetoacetate, and beta-3-hydroxybutyrate.
Beta-3-hydroxybutyrate contributes most prominently to an anion gap metabolic
acidosis.

Patients with HHS have some pancreatic beta cell function, and the degree of lipolysis
required to produce a measurable ketonemia may not occur.

HHS dia masih memiliki insulin yang cukup untuk mencegah lipolisis tetapi tidak untuk
mempertahan kadar glukosa.

HHS is characterized
by severe hyperglycemic diuresis and dehydration, hypernatremia, minimal to absent
ketonemia, and serum osmolality of >320 mOsm/kg.

Because of severe hypernatremia and elevated serum osmolality, HHS patients more
often present with severe mental status changes, including coma

DKA is both a systemic inflammatory illness and a cause of vascular endothelial injury
that can result in disseminated intravascular coagulation and pulmonary interstitial
edema, as well as hypercoagulable
pathologies, such as stroke, pulmonary embolism, and dural sinus thrombosis